Aquaporin-4 deficiency down-regulates glutamate uptake and GLT-1 expression in astrocytes

作者：Zeng, Xiao-Ning; Sun, Xiu-Lan; Gao, Lin; Fan, Yi; Ding, Jian-Hua; Hu, Gang^*

来源：Molecular and Cellular Neuroscience, 2007, 34(1): 34-39.

DOI：10.1016/j.mcn.2006.09.008

• WATER TRANSPORT
• BRAIN EDEMA
• GLIAL-CELLS
• MECHANISMS
• CHANNEL
• BLOOD
• MICE
• PHENOTYPE
• DELETION
• LACKING

The role of aquaporin-4 in water transport has been extensively investigated, while little information exists regarding its contribution to astrocytic functions such as the action to glutamatergic transmission. Since aquaporin-4 has been detected widely co-localized with glutamate transporter 1 (GLT-1) and glutamate transporters also present water transport properties, we investigated the regulative role of aquporin-4 on glutamate transporter using primary cultured astrocytes from aquaporin-4 knockout (AQP4(-/-)) mice. It was demonstrated that lack of aquaporin-4 down-regulated astrocytic expression of GLT-1 but not of glutamate/aspartate transporter (GLAST). The result from [H-3]D,L-glutamate uptake analysis showed a lower uptake capability in AQP4-/- astrocytes. Furthermore, MTT and LDH assays indicated less cellular toxicity induced by excessive glutamate in AQP4(-/-) genotype. These findings provide direct evidences for the first time that aquaporin-4 plays an important role in the function of glutamate transporters. And the present study will improve our understanding of aquaporin-4-glutamanergic biology.

• 出版日期2007-1
• 单位南京医科大学